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  • Articles  (19,842)
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  • Articles  (19,842)
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  • 1
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    Ubiquitin-dependent rapid degradation conceals a cell-protective function of cytoplasmic SIRT3 against oxidative stress (2021)
    Oxford University Press
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    Publication Date: 2021-10-29
    Description: SIRT3 is an NAD+-dependent protein deacetylase localized in mitochondria. Several studies reported localization of SIRT3 in the cytoplasm or nucleus, but data of these studies were not consistent. We detected expression of mitochondrial (SIRT3mt) and cytoplasmic (SIRT3ct) Sirt3 mRNAs in the mouse brain, and we also found SIRT3 immunostaining of mitochondria and cytoplasm in the brain and cultured neural cells. However, expression levels of SIRT3ct in COS cells transfected with SIRT3ct cDNA were much lower than those of SIRT3mt. We found that SIRT3ct but not SIRT3mt was promptly degraded by ubiquitin-dependent degradation, in which SIRT3ct degradation was mediated mainly by ubiquitination of NH2-terminal methionine and partly by that of lysine residues of SIRT3ct. SIRT3ct expression level was significantly enhanced by treatment of cells with staurosporine or H2O2. H2O2 treatment promoted nuclear translocation of SIRT3ct and induced histone H3 deacetylation and superoxide dismutase 2 expression. Overexpression of SIRT3ct decreased cell death caused by H2O2 at levels similar to those achieved by overexpression of SIRT3mt. Knockdown of Sirt3 mRNA increased cell death caused by amyloid-β (Aβ), and overexpression of SIRT3ct suppressed the toxic function of Aβ in PC12 cells. These results indicate that SIRT3ct promotes cell survival under physiological and pathological conditions.
    Print ISSN: 0021-924X
    Electronic ISSN: 1756-2651
    Topics: Biology , Chemistry and Pharmacology
    Published by Oxford University Press on behalf of Japanese Biochemical Society.
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  • 2
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    Crystallographic studies of cytochrome c and cytochrome c oxidase (2021)
    Oxford University Press
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    Publication Date: 2021-10-26
    Description: I started on crystallographic studies of cytochrome c (Cyt.c) in the later 1960s at Institute for Protein Research, Osaka University. The institute successfully built the structural model of ferro-Cyt.c by the multiple heavy atom replacement method in the early 1970s. In the early 1990s, crystals of cytochrome c oxidase (CcO) from bovine heart were obtained by using polyethylene glycol 4000 (Sigma) as the precipitant. We reported the first structure of a mammalian membrane protein at 2.8 Å resolution in 1995. High-resolution crystallography of CcO is in progress to understand the coupling mechanism of O2 reduction and proton pumping. We determined the structure of the mammalian Cyt.c–CcO complex at 2.0 Å resolution and identified the “soft and specific” interaction between Cyt.c and CcO, which effected high-efficiency inter-molecular electron transfer.
    Print ISSN: 0021-924X
    Electronic ISSN: 1756-2651
    Topics: Biology , Chemistry and Pharmacology
    Published by Oxford University Press on behalf of Japanese Biochemical Society.
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  • 3
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    NGLY1: Insights from C. elegans (2021)
    Oxford University Press
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    Publication Date: 2021-10-26
    Description: Summary Peptide:N-glycanase is an evolutionarily conserved deglycosylating enzyme that catalyzes the removal of N-linked glycans from cytosolic glycoproteins. Recessive mutations that inactivate this enzyme cause NGLY1 deficiency, a multisystemic disorder with symptoms including developmental delay and defects in cognition and motor control. Developing treatments for NGLY1 deficiency will require an understanding of how failure to deglycosylate NGLY1 substrates perturbs cellular and organismal function. In this review, I highlight insights into peptide:N-glycanase biology gained by studies in the highly tractable genetic model animal C. elegans. I focus on the recent discovery of SKN-1A/Nrf1, an N-glycosylated transcription factor, as a peptide:N-glycanase substrate critical for regulation of the proteasome. I describe the elaborate post-translational mechanism that culminates in activation of SKN-1A/Nrf1 via NGLY1-dependent ‘sequence editing’ and discuss the implications of these findings for our understanding of NGLY1 deficiency.
    Print ISSN: 0021-924X
    Electronic ISSN: 1756-2651
    Topics: Biology , Chemistry and Pharmacology
    Published by Oxford University Press on behalf of Japanese Biochemical Society.
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  • 4
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    GlcNAc-Asn (GNA) is a biomarker for NGLY1 deficiency (2021)
    Oxford University Press
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    Publication Date: 2021-10-26
    Description: Substrate derived biomarkers are necessary in slowly progressing monogenetic diseases caused by single enzyme deficiencies to identify affected patients and serve as surrogate markers for therapy response. N-glycanase 1 (NGLY1) deficiency is an ultra-rare autosomal recessive disorder characterized by developmental delay, peripheral neuropathy, elevated liver transaminases, hyperkinetic movement disorder, and (hypo)-alacrima. We demonstrate that N-acetylglucosamine-asparagine (GlcNAc-Asn; GNA), is the analyte most closely associated with NGLY1 deficiency, showing consistent separation in levels between patients and controls. GNA accumulation is directly linked to the absence of functional NGLY1, presenting strong potential for its use as a biomarker. In agreement, a quantitative LC-MS/MS assay, developed to assess GNA from 3 to 3000 ng/mL, showed it is conserved as a marker for loss of NGLY1 function in NGLY1 deficient cell lines, rodents (urine, cerebrospinal fluid, plasma, and tissues), and patients (plasma and urine). Elevated GNA levels differentiate patients from controls, are stable over time, and correlate with changes in NGLY1 activity. GNA as a biomarker has the potential to identify and validate patients with NGLY1 deficiency, act as a direct pharmacodynamic marker, and serve as a potential surrogate endpoint in clinical trials.
    Print ISSN: 0021-924X
    Electronic ISSN: 1756-2651
    Topics: Biology , Chemistry and Pharmacology
    Published by Oxford University Press on behalf of Japanese Biochemical Society.
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  • 5
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    Genome-wide distribution of 5hmC in the dental pulp of mouse molars and incisors (2021)
    Oxford University Press
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    Publication Date: 2021-10-22
    Description: The dental pulp is critical for the production of odontoblasts to create reparative dentin. In recent years dental pulp has become a promising source of mesenchymal stem cells that are capable of differentiating into multiple cell types. To elucidate the transcriptional control mechanisms specifying the early phases of odontoblast differentiation, we analyzed the DNA demethylation pattern associated with 5-hydroxymethylcytosine (5hmC) in the primary murine dental pulp. 5hmC plays an important role in chromatin accessibility and transcriptional control by modeling a dynamic equilibrium between DNA methylation and demethylation. Our research revealed 5hmC enrichment along genes and non-coding regulatory regions associated with specific developmental pathways in the genome of mouse incisor and molar dental pulp. Although the overall distribution of 5hmC is similar, the intensity and location of the 5hmC peaks significantly differs between the incisor and molar pulp genome, indicating cell type-specific epigenetic variations. Our study suggests that the differential DNA demethylation pattern could account for the distinct regulatory mechanisms underlying the tooth-specific ontogenetic programs.
    Print ISSN: 0021-924X
    Electronic ISSN: 1756-2651
    Topics: Biology , Chemistry and Pharmacology
    Published by Oxford University Press on behalf of Japanese Biochemical Society.
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  • 6
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    Forty years of the structure of plant-type Ferredoxin (2021)
    Oxford University Press
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    Publication Date: 2021-10-18
    Description: The X-ray structure of a [2Fe-2S]-type Ferredoxin from Spirulina platensis, solved by a collaborative group led by Profs Masao Kakudo, Yukiteru Katsube and Hiroshi Matsubara, was the first high-resolution structure of a plant-type Ferredoxin deposited in the Protein Data Bank. The main chain structure, comprising a [2Fe-2S] cluster ligated by four conserved cysteine residues, together with a molecular evolutionary study based on a series of amino acid sequence determinations, was reported in Nature in 1980. The consequent detailed crystallographic analysis, including crystallization, heavy atom derivatization, data collection, phase calculation, and model building, was published by the same group in the Journal of Biochemistry in 1981. The pioneering X-ray analysis of S. platensis Ferredoxin at 2.5 Å resolution was a key milestone in structural research on the photosynthetic electron transport chain, informing related and challenging studies on other components of the photosynthetic electron transfer chain.
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    Topics: Biology , Chemistry and Pharmacology
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  • 7
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    The dedicated chaperones of eL43, Puf6 and Loc1, can also bind RPL43 mRNA and regulate the production of this ribosomal protein (2021)
    Oxford University Press
    Details
    Publication Date: 2021-10-18
    Description: The level of ribosome biogenesis is highly associated with cell growth rate. Because many ribosomal proteins have extraribosomal functions, overexpression or insufficient supply of these proteins may impair cellular growth. Therefore, the supply of ribosomal proteins is tightly controlled in response to rRNA syntheses and environmental stimuli. In our previous study, 2 RNA-binding proteins, Puf6 and Loc1, were identified as dedicated chaperones of the ribosomal protein eL43, with which they associate to maintain its protein level and proper loading. In this study, we demonstrate that Puf6 and Loc1 interact with RPL43 mRNA. Notably, Puf6 and Loc1 usually function as a dimeric complex to bind other mRNAs; however, in this instance, the individual proteins, but not the complex form, can bind RPL43 mRNA. Thus, Puf6 or Loc1 could bind RPL43 mRNA in loc1Δ or puf6Δ, respectively. The binding of Puf6 or Loc1 caused negative effects for eL43 production: decreased RNA stability and translation of RPL43A/B mRNA. The present results suggest that these dedicated chaperones control the protein levels of eL43 from the standpoint of stability and through regulating its production.
    Print ISSN: 0021-924X
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    Topics: Biology , Chemistry and Pharmacology
    Published by Oxford University Press on behalf of Japanese Biochemical Society.
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  • 8
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    Capn4 aggravates angiotensin II-induced cardiac hypertrophy by activating the IGF-AKT signalling pathway (2021)
    Oxford University Press
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    Publication Date: 2021-09-27
    Description: Capn4 belongs to a family of calpains that participate in a wide variety of biological functions, but little is known about the role of Capn4 in cardiac disease. Here, we show that the expression of Capn4 was significantly increased in Angiotensin II (Ang II)-treated cardiomyocytes and Ang II-induced cardiac hypertrophic mouse hearts. Importantly, in agreement with the Capn4 expression patterns, the maximal calpain activity measured in heart homogenates was elevated in Ang II-treated mice and oral coadministration of SNJ-1945 (calpain inhibitor) attenuated the total calpain activity measured in vitro. Functional assays indicated that overexpression of Capn4 obviously aggravated Ang II-induced cardiac hypertrophy, whereas Capn4 knockdown resulted in the opposite phenotypes. Further investigation demonstrated that Capn4 maintained the activation of the insulin-like growth factor (IGF)-AKT signalling pathway in cardiomyocytes by increasing c-Jun expression. Mechanistic investigations revealed that Capn4 directly bound and stabilized c-Jun and knockdown of Capn4 increased the ubiquitination level of c-Jun in cardiomyocytes. Additionally, our resultsGraphical Abstract$includegraphics{ wartpath mvab100fx1}$ demonstrated that the antihypertrophic effect of Capn4 silencing was partially dependent on the inhibition of c-Jun. Overall, these data suggested that Capn4 contributes to cardiac hypertrophy by enhancing the c-Jun-mediated IGF-AKT signalling pathway and could be a potential therapeutic target for hypertrophic cardiomyopathy.
    Print ISSN: 0021-924X
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    Topics: Biology , Chemistry and Pharmacology
    Published by Oxford University Press on behalf of Japanese Biochemical Society.
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  • 9
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    Human TRPV1 and TRPA1 are receptors for bacterial quorum sensing molecules (2021)
    Oxford University Press
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    Publication Date: 2021-09-23
    Description: In this study, we investigated the activation of TRPV1 and TRPA1 by N-acyl homoserine lactones, quorum sensing molecules produced by Gram-negative bacteria, and the inhibitory effect of TRPV1 and TRPA1 by autoinducing peptides (AIPs), quorum sensing molecules produced by Gram-positive bacteria, using human embryonic kidney 293T cell lines stably expressing human TRPV1 and TRPA1, respectively. As a result, we found that some N-acyl homoserine lactones, such as N-octanoyl-L-homoserine lactone (C8-HSL), N-nonanoyl-L-homoserine lactone (C9-HSL) and N-decanoyl-L-homoserine lactone (C10-HSL), activated both TRPV1 and TRPA1. In addition, we clarified that some N-acyl homoserine lactones, such as N-3-oxo-dodecanoyl-L-homoserine lactone (3-oxo-C12-HSL), only activated TRPV1 and N-acyl homoserine lactones having saturated short acyl chain, such as N-acetyl-L-homoserine lactone (C2-HSL) and N-butyryl-L-homoserine lactone (C4-HSL), only activated TRPA1. Furthermore, we found that an AIP, simple linear peptide CHWPR, inhibited both TRPV1 and TRPA1 and peptide having thiolactone ring DICNAYF, the thiolactone ring were formed between C3 to F7, strongly inhibited only the TRPV1. Although the specificity of TRPV1 and TRPA1 for quorum sensing molecules was different, these data suggest that both TRPV1 and TRPA1 would function as receptors for quorum sensing molecule produced by bacteria.Graphical Abstract
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    Topics: Biology , Chemistry and Pharmacology
    Published by Oxford University Press on behalf of Japanese Biochemical Society.
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  • 10
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    Nucleosome assembly protein 1 (NAP-1) is a regulator of histone H1 acetylation (2021)
    Oxford University Press
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    Publication Date: 2021-09-22
    Description: Acetylation of histone H1 is generally considered to activate transcription, whereas deacetylation of H1 represses transcription. However, the precise mechanism of the acetylation is unknown. Here, using chromatography, we identified nucleosome assembly protein 1 (NAP-1) as having inhibitory activity against histone H1 acetylation by acetyltransferase p300. We found that native NAP-1 interacts with H1 in a Drosophila crude extract. We also found that it inhibits the deacetylation of histone H1 by histone deacetylase 1 (HDAC1). The core histones in nucleosomes were acetylated in a GAL4–VP16 transcriptional activator-dependent manner in vitro. This acetylation was strongly repressed by hypoacetylated H1 but to a lesser extent by hyperacetylated H1. Consistent with these findings, a micrococcal nuclease assay indicated that hypoacetylated H1, which represses activator-dependent acetylation, was incorporated into chromatin, whereas hyperacetylated H1 was not. To determine the contribution of NAP-1 to transcriptional regulation in vivo, we compared NAP-1 knockdown (KD) with coactivator CREB-binding protein (CBP) KD using RNA sequencing in Drosophila Schneider 2 cells. Most genes were downregulated rather than upregulated by NAP-1 KD, and those downregulated genes were also downregulated by CBP KD. Our results suggest that NAP-1 plays a role in transcriptional regulation by fine-tuning the acetylation of histone H1.
    Print ISSN: 0021-924X
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    Topics: Biology , Chemistry and Pharmacology
    Published by Oxford University Press on behalf of Japanese Biochemical Society.
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